Leptin is a key biological marker related to energy balance and development of diabetes and cardiovascular diseases. Its levels are increased in populations with a high degree of the metabolic syndrome. Life history of evolution has, however, largely taken place under the ecological context of hunting and gathering. In this study, we explored whether the first steps of transition to sedentary agriculture involve a change of body composition, plasma leptin concentration, and markers of the metabolic syndrome. A total of 59 healthy Shuar Amerindian women living in 5 isolated communities in the Ecuadorian Amazonian rain forest were examined. Women (n = 33) from the largest and oldest community, Yuwientsa, who are more dependent on agriculture had higher fat mass (11.7 ± 3.3 v 14.5 ± 4.0 kg; P = .023) but the same body mass index (24.1 ± 2.7 v 23.1 ± 2.8 kg/m2; not significant [NS]) and lean body mass (41.0 ± 5.0 v 40.2 ± 6.2 kg; NS) than women (n = 26) from the 4 traditional hunter/gather settlements. Furthermore, women from Yuwientsia had higher leptin (5.5 ± 3.1 v 4.1 ± 2.7 ng/mL; P = .021) and plasma insulin levels (49.8 ± 37.4 v 35.5 ± 12.7 pmol/L; P = .013). Homeostasis model assessment (HOMA) values (8.8 ± 4.8 v 6.1 ± 2.2; P = .004) and plasma triglyceride levels (2.3 ± 1.0 v 1.7 ± 0.6 mmol/L; P = .025) as markers of the metabolic syndrome were also increased in the Yuwientsa population. Mean plasma glucagon concentrations were not different between the groups. We conclude that body fat and levels of insulin and leptin are higher in the population more dependent on agriculture for living. In fact, the leptin concentrations from the 4 hunter/gather communities are the lowest mean value ever reported from a population of healthy females. As there are no genetic or biologic differences between the Shuar Indians from the 5 communities, we hypothesize that behavioral responses to a changing environment may be the key to the development of the metabolic syndrome and elevated plasma leptin concentrations.
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Accepted: April 9, 2004
Received: January 22, 2004
☆Supported by Grant No. 6834 from the Swedish Research Council, Albert Pahlsson Foundation, Swedish Diabetes Association, and Stiftelsen för forskning inom diabetes och kärlsjukdom.
© 2004 Elsevier Inc. Published by Elsevier Inc. All rights reserved.